We further showed that the deletion of DOT1L1, the sole H3K79 methyltransferase, impeded leukemia cell proliferation as well as switched exon skipping to the inclusion isoform in two MLL-rearranged acute myeloid leukemia cell lines. (springer.com)

19 , 20 As a result, MLL-fusion proteins gain the ability to recruit DOT1L to MLL target genes where the resulting hypermethylation at H3K79 leads to aberrant expression of a characteristic set of genes including HOXA9 and MEIS1 that drive leukemogenesis. (bloodjournal.org)